Monokine-Producing Cells Predominate in the Recruitment Phase of NOD Insulitis while Cells Producing Th1-type Cytokines Characterize the Effector Phase

Pilström, Björn; Björk, Lars; Böhme, Jan

doi:10.1006/jaut.1996.0115

Cited by 18 publications

(6 citation statements)

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“…Macrophages are probably the first cell type to infiltrate the islets in the early stages of insulitis in NOD mice, followed by T lymphocytes [15,55]. This initial prediabetic phase is associated with the local production of pro-inflammatory cytokines, especially IL-1b, IL-6, IFN-g and TNF-a [15,56]. This could explain our observations of increased MCP-1 expression in NOD islets.…”

Section: Discussionmentioning

confidence: 70%

Monocyte chemoattractant protein-1 is expressed in pancreatic islets from prediabetic NOD mice and in interleukin-1β-exposed human and rat islet cells

et al. 2001

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Section: Discussionmentioning

confidence: 70%

Monocyte chemoattractant protein-1 is expressed in pancreatic islets from prediabetic NOD mice and in interleukin-1β-exposed human and rat islet cells

et al. 2001

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“…Studies about the correlation of diabetes and T helper cell phenotypes lead to the idea that Th1 and their cytokines promote diabetes [374, 375]. Th1 cells can either cause β-cell destruction directly [376, 377] or by secreting Th1 cytokine (INF-γ) to recruit and activate macrophages and CD8+ T lymphocytes that exert toxic functions [378]. In contrast, Th2, through secretion of the cytokine IL-4, is generally considered protective [375, 379].…”

Section: The Pathogenesis Of T1dmentioning

confidence: 99%

Regulation of Insulin Synthesis and Secretion and Pancreatic Beta-Cell Dysfunction in Diabetes

Fu¹,

Gilbert²,

Liu³

2013

Current Diabetes Reviews

684

443

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Pancreatic β-cell dysfunction plays an important role in the pathogenesis of both type 1 and type 2 diabetes. Insulin, which is produced in β-cells, is a critical regulator of metabolism. Insulin is synthesized as preproinsulin and processed to proinsulin. Proinsulin is then converted to insulin and C-peptide and stored in secretary granules awaiting release on demand. Insulin synthesis is regulated at both the transcriptional and translational level. The cis-acting sequences within the 5′ flanking region and trans-activators including paired box gene 6 (PAX6), pancreatic and duodenal homeobox-1(PDX-1), MafA, and B-2/Neurogenic differentiation 1 (NeuroD1) regulate insulin transcription, while the stability of preproinsulin mRNA and its untranslated regions control protein translation. Insulin secretion involves a sequence of events in β-cells that lead to fusion of secretory granules with the plasma membrane. Insulin is secreted primarily in response to glucose, while other nutrients such as free fatty acids and amino acids can augment glucose-induced insulin secretion. In addition, various hormones, such as melatonin, estrogen, leptin, growth hormone, and glucagon like peptide-1 also regulate insulin secretion. Thus, the β-cell is a metabolic hub in the body, connecting nutrient metabolism and the endocrine system. Although an increase in intracellular [Ca2+] is the primary insulin secretary signal, cAMP signaling-dependent mechanisms are also critical in the regulation of insulin secretion. This article reviews current knowledge on how β-cells synthesize and secrete insulin. In addition, this review presents evidence that genetic and environmental factors can lead to hyperglycemia, dyslipidemia, inflammation, and autoimmunity, resulting in β-cell dysfunction, thereby triggering the pathogenesis of diabetes.

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“…Additional recent publications also seem to argue against Fas‐mediated thyroid suicide (as proposed by Giordano et al., 1997). Mice genetically manipulated to specifically over‐express FasL in the thyroid do not have increased apoptosis in thyroid cells (Batteux et al . 1999, Batteux et al .…”

Section: Receptor‐mediated Apoptosis In Thyroid Cellsmentioning

confidence: 99%

Apoptosis and autoimmune thyroid disease: following a TRAIL to thyroid destruction?

Bretz

Baker

2001

Clinical Endocrinology

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Monokine-Producing Cells Predominate in the Recruitment Phase of NOD Insulitis while Cells Producing Th1-type Cytokines Characterize the Effector Phase

Cited by 18 publications

References 0 publications

Monocyte chemoattractant protein-1 is expressed in pancreatic islets from prediabetic NOD mice and in interleukin-1β-exposed human and rat islet cells

Monocyte chemoattractant protein-1 is expressed in pancreatic islets from prediabetic NOD mice and in interleukin-1β-exposed human and rat islet cells

Regulation of Insulin Synthesis and Secretion and Pancreatic Beta-Cell Dysfunction in Diabetes

Apoptosis and autoimmune thyroid disease: following a TRAIL to thyroid destruction?

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